Estradiol and progesterone receptor concentrations and 17 beta-hydroxysteroid-dehydrogenase activity in estrogen-progestin stimulated endometrium of women with gonadal dysgenesis.
Four hypergonadotrophic women between 25 and 37 years of age with gonadal dysgenesis were treated sequentially with estrogens and a progestin. The hormonal environment induced by this therapy was similar to that of ovulating women, as demonstrated by serum levels of estradiol, endometrial histology and pituitary gonadotropin secretion before and after LH-RH double stimulation. The concentrations of estradiol and progesterone receptors (ER and PR) and the activity of the 17 beta-hydroxysteroid-dehydrogenase (17 beta-HSD) were determined in endometrial curettings obtained from the above patients at 5 different days of their 28-day artificial cycles. The results were correlated to the histology of the endometrium and the serum concentrations of estradiol at the corresponding days of the cycle. The cytoplasmic ER and PR concentrations in the endometrium were 3-6 times higher during the estrogen than progestin phase of the induced endometrial cycle. For the activity of the 17 beta-HSD, the contrary was the case, being 6-10 fold higher during the progestin phase. A 22-day administration of estrogens only did not lead to a rise in enzyme activity or decrease in receptor content as observed under progestin influence after day 14. Since ER and PR concentrations and 17 beta-HSD activities were similar to those in the endometrium of normally ovulating women, these results confirm experimentally the present concept concerning the dependence of the cytoplasmic ER and PR content and 17 beta-HSD activity on female sex hormone action.
D042842:11-beta-Hydroxysteroid Dehydrogenases; D000328:Adult; D004717:Endometrium / Q000378:metabolism*; D004958:Estradiol / Q000378:metabolism* / Q000627:therapeutic use; D004964:Estriol / Q000627:therapeutic use; D004967:Estrogens / Q000627:therapeutic use*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D006059:Gonadal Dysgenesis / Q000235:genetics / Q000378:metabolism* / Q000628:therapy; D006801:Humans; D006913:Hydroxysteroid Dehydrogenases / Q000378:metabolism*; D007621:Karyotyping; D007986:Luteinizing Hormone / Q000097:blood; D008524:Medrogestone / Q000627:therapeutic use*; D011245:Pregnadienes / Q000627:therapeutic use*; D011959:Receptors, Estradiol; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism*
D004967:Estrogens; D011245:Pregnadienes; D011959:Receptors, Estradiol; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D008524:Medrogestone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D006913:Hydroxysteroid Dehydrogenases; D042842:11-beta-Hydroxysteroid Dehydrogenases; D004964:Estriol